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D M Nance

Publications and source records attributed to D M Nance.

99 records · Page 6Linked to original sources
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Modifications in gonadotropin control and reproductive behavior in the female rat by hypothalamic and preoptic lesions.

Effects of small hypothalamic and preoptic area lesions on vaginal cyclicity, ovulation and ovarian weights of female rats were examined. Animals were then gonadectomized and tested for lordosis behavior following injections of estrogen alone and estrogen plus progesterone. Male sex behavior was also measured during daily treatment with testosterone. Relative to sham operated rats, lesions in the dorsal preoptic area produced a significant increase in lordosis behavior, virtual elimination of male sex behavior, and only marginal effects on ovarian function. Animals with lesions in the ventral preoptic area showed constant vaginal cornification, lack of ovulation and significantly smaller ovaries than the other groups. These rats also tended to show more female sex behavior and less male sex behavior than sham operated rats. Animals with lesions in the anterior hypothalamus and dorsomedial hypothalamus showed normal ovarian function and levels of female and male sex behavior comparable to the ventral preoptic lesioned rats. Animals with lesions in the ventromedial hypothalamus tended to show lower levels of lordosis behavior than sham animals but displayed a dramatic and significant increase in male copulatory behavior relative to the other groups. These data indicate a clear dissociation between the neural control of cyclic gonadotropin activity and sex specific reproductive behavior.

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Similar effects of estrogen and lateral hypothalamic lesions on feeding behavior of female rats.

Many similarities exist between the inhibitory influence of estrogen on food intake (FI) and body weight (BWt) in female rats and the effect of lateral hypothalamic (LH) lesions on energy balance. Thus, a possible interaction of small electrolytic LH lesions (0.8 mA/10 sec) with hormone-dependent changes in FI, BWt and feeding patterns of female rats was examined. Relative to sham operated controls, rats with LH lesions showed a transitory period of anorexia and initial loss of BWt. Subsequently, FI and BWt gains of lesioned rats returned to control levels although a small chronic reduction in mean BWt was observed relative to sham animals. Daily changes in FI and BWt during 4-day estrous cycles as well as post-ovariectomy increases in FI and BWt were comparable for lesion and sham animals. Also, both groups showed a similar decrease in FI and BWt following a SC injection of estradiol benzoate (EB). Possible effects of LH lesions were further examined by analyzing feeding patterns. Feeding behavior was continuously monitored with photodetectors and recorded on an Esterline Angus event marker before and after a single SC injection of 6 micrograms of EB. Relative to shams, LH animals showed an exaggerated diurnal distribution of meals, ate smaller meals of shorter duration and had larger intervals between meals during the light period. EB was found to shift the feeding patterns of sham animals towards the meal patterns shown by the lesioned rats (exaggerated diurnal distribution of meals, etc.). However, the lesioned rats also showed a normal change in feeding patterns following EB, albeit these changes occurred from a markedly different baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of estrogen upon hypothalamic vulnerability to goldthioglucose in mice.

Two groups of ovariectomized albino mice were given subcutaneous injections of either seasame oil or increasing doses of estradiol benzoate (EB) for 8 days. Mice were housed in groups of three; food intake (FI) and body weight (Bwt) were measured daily during this period. After 8 days, all mice were injected IP with 0.3 mg/g of goldthioglucose (GTG) and sacrificed 2 days later. The extent of hypothalamic damage after GTG was assessed histologically. Although EB did not depress FI or Bwt, perhaps because of some behavioral interaction within the groups of mice, the extent of hypothalamic damage after GTG was significnatly increased in EB-treated mice relative to that of oil-injected controls. These data support the view that estrogen may enhance the uptake and/or storage of glucose by the ventromedial hypothalamus.

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Further characterization of fat diet-induced changes in responsiveness to estrogen and glucose.

Possible reasons for hyperresponsiveness to the anorexic influence of estrogen of rats fed a high-fat (F) diet were explored. It was found that (1) hyperresponsiveness appeared unrelated to body weight, (2) other estrogenic effects (upon vaginal epithelia and upon mating behavior) were normal in F-fed rats, (3) hyperresponsiveness to estrogen was not a result of alterations in brain dopamine or norepinephrine, (4) F-fed rats were also hyperresponsive to postabsorptive satiating effects of intragastric glucose loads. Thus, an altered glucose metabolism of F-fed rats may be related to an increased responsiveness to the anorexic effects of estrogen.

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Effects of diet upon hypothalamic vulnerability to goldthioglucose in male mice.

Three groups of male mice were fed three different diets for about 3 weeks: powdered chow (C), a high fat (F) diet (chow:Crisco, 2:1), and a high dextrose (D) diet (chow:dextrose, 2:1). Food and water intake and body weights (BWts) were measured daily. On Day 20 of the study, mice were injected IP with 0.3 mg/g of goldthioglucose (GTG). Two days later, the mice were sacrificed and brains were removed for histological examination of GTG-induced lesions in the ventromedial hypothalamus (VMH). It was found that (1) F-fed mice ate more and gained more BWt than C- and D-fed mice, and (2) the average GTG lesion volume of F-fed mice was twice as large as those of C- and D-fed mice. In view of known alterations in sensitivity of the VMH to goldthioglucose with changes in glucose metabolism, it is suggested that the larger goldthioglucose induced lesions in F-fed mice may be due to elevated blood levels of goldthioglucose or altered glucose metabolism in goldthioglucose sensitivity cells in the VMH.

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Effects of septal lesions and chronic estrogen treatment on dopamine, GABA and lordosis behavior in male rats.

Septal lesions (SL) in female rats result in an increased sensitivity to the behavioral effects of acute estradiol benzoate (ACUTE-EB; 2 microgram/day X 3) treatment as measured by the lordosis quotient (LQ: number of lordotic responses X 100/number of mounts). Male rats, intact or castrated, do not show this enhanced behavioral response to ACUTE-EB unless they are treated with EB (2 microgram/day) for 2--4 weeks immediately following the production of SL. The present study was undertaken to examine possible neurochemical alterations which could account for the enhanced behavioral sensitivity to ACUTE-EB seen in the SL male rat treated chronically with EB during the postlesion period (SL-EB). Three groups, normal males, SL-EB and SL males chronically treated with oil (SL-oil), were subdivided and treated with ACUTE-EB or oil and decapitated. The brains were removed, frozen and stored at -50 degrees C prior to dissection and assay. Tyrosine hydroxylase (TH) activity was assayed in the dopamine (DA) rich areas of the forebrain (striatum, STR, nucleus accumbens septi, ACB; and olfactory tubercle). The TH activity was significantly suppressed in both the STR and ACB of the SL-EB males treated with ACUTE-EB. The glutamic acid decarboxylase (GAD) activity in both the substantia nigra and ventral tegmentum was significantly increased in the SL-EB males given ACUTE-EB relative to that of all other groups. In summary, SL-EB males given ACUTE-EB show (1) an enhanced LQ, (2) decreased TH activity in the region of DA terminals, and (3) increased GAD activity in the region of DA cell bodies. The increase in GAD activity is suggested to be a result of an altered neuronal feedback because of plastic changes that occur during chronic EB treatment following production of SL. This probable increase in inhibitory tone in the region of the DA cell bodies may explain the observation that the SL-EB male exhibits decreased DA turnover following ACUTE-EB treatment. Moreover, since DA may be inhibitory to the display of lordosis behavior, the SL-EB males may show an enhanced LQ, at least partially, because of this reduction in DA activity.

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Reduced ovarian function and lordosis behavior following hypothalamic knife cuts.

Lordosis behavior (LQ) estrous cycles and ovarian status were studied in the same animals following either frontal (FC), frontolateral (FLC) or sham (S) surgical interruption of medial basal hypothalamic (MBH) neural connections made with a modified Halász knife (1.5 mm radius). LQ was studied in adult female rats at 7, 30, 105 and 180 day after FC, FLC or S and estrous cycles were monitored for 28 day after cuts. Vaginal cytology examined before and after S surgery indicated regular 4-5 day cycles, whereas after FC vaginal cytology became predominately cornified and after FLC it was variable. Ovarian weights and appearance at ovariectomy (OVX) supported cycle data: S ovaries had recent corpora lutea (CL); FC gonads were smaller with no recent CL and FLC gonads appeared atrophic. Multiple regression analysis of individual FC and FLC dimensions indicated that cut location and dimensions contributed significantly to the length of postoperative estrus periods. After OVX all animals were tested for LQ after estradiol benzoate (EB) and EB plus progesterone (P) priming. Although there were no group LQ differences after EB alone, S and FC animals showed an increase in LQ after EB plus P, whereas, FLC rats showed no change and this effect persisted for 180 day. Multiple regression analysis of FC and FLC coordinates indicated that the more posterior and lateral extending cuts were associated with lower LQ scores. Collectively, these data suggest a role for similar anterolateral MBH neural connections in (1) basal and cyclic gonadotrophin release and (2) EB plus P effects on lordosis behavior.

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Neuroendocrine control of ovarian autografts.

At 24 days of age, either one or both ovaries of female rats were removed and transplanted subcutaneously on their respective side. Relative to sham operated rats, endocrine effects of the ovarian grafts were as follows: 1) Animals with ovarian grafts showed an advancement of puberty, 2) rats with bilateral grafts showed more 5 day estrous cycles and higher FSH levels, 3) hemi-ovariectomy of animals with bilateral grafts produced a greater increase in both LH and FSH 6-8 hr post-surgery in contrast to controls which only showed an increase in serum FSH levels, 4) weights of the bilateral grafts were comparable to intact ovaries, but the unilateral grafts were small and comparable to their original size at the time of transplantation (the intact ovary showing compensatory hypertrophy), 5) both control and bilateral ovarian graft groups showed ovarian compensatory hypertrophy, 6) removal of the small unilateral ovarian graft had no detectable endocrine effect on the remaining intact ovary which had already undergone compensatory hypertrophy, 7) removal of the intact ovary of rats with a unilateral graft produced a remarkable increase in the weight of the remaining small autograft such that these animals had the largest remaining gonad as well as higher uterine weights than controls. Thus, although ovarian autografts appear to function similar to in situ glands, the alterations in puberty, estrous cycles, FSH and LH levels and uterine weights suggest that endocrine control mechanisms are altered in rats with ovarian grafts.

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